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Themed Issue papers |
1 Departments of Pharmacodynamics, College of Pharmacy2 Physiology and Functional Genomics, College of Medicine, University of Florida, Gainesville, FL 32610, USA
Less than one-third of patients with hypertension have their blood pressures (BP) controlled with current traditional therapeutic approaches for the treatment and control of hypertension. Pharmacological approaches may have reached a plateau in their effectiveness and thus newer innovative strategies need to be studied not only to increase the number of patients that can achieve BP control, but also to find a way to cure, not just manage, the disease. Continuous advances in gene delivery systems coupled with the completion of the Human Genome Project, now make it possible to investigate genetic means for the treatment and possible cure for hypertension. The renin–angiotensin system (RAS) has long been known to regulate BP, and salt and water metabolism. This system is unique in having both a peripheral circulating system and a tissue-based system. Each of these components have been ascribed a variety of physiological effects that have been associated with not only an increase in BP, but also in a variety of the pathophysiological manifestations associated with hypertension, such as cardiac hypertrophy and kidney dysfunction. We and others have used an antisense gene therapy approach, targeting the classical components of the RAS, to effectively attenuate the development of hypertension and related cardiovascular pathophysiologies in numerous experimental models of hypertension. Recently other components of the RAS have been elucidated and some of these components may be potential targets in a gene therapy approach. This article will focus on angiotensin-converting enzyme 2 (ACE2) as a new, potential target of gene therapy for hypertensive disorders.
(Received 4 November 2004;
accepted after revision 5 January 2005; first published online 7 January 2005)
Corresponding author M. J. Katovich: Department of Pharmacodynamics, University of Florida, College of Pharmacy, PO Box 100487, Gainesville, FL 32610-0487, USA. Email: katovich{at}cop.ufl.edu
This article has been cited by other articles:
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  M. Yamazato, Y. Yamazato, C. Sun, C. Diez-Freire, and M. K. Raizada Overexpression of Angiotensin-Converting Enzyme 2 in the Rostral Ventrolateral Medulla Causes Long-Term Decrease in Blood Pressure in the Spontaneously Hypertensive Rats Hypertension, April 1, 2007; 49(4): 926 - 931. [Abstract] [Full Text] [PDF]
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 C. Diez-Freire, J. Vazquez, M. F. Correa de Adjounian, M. F. R. Ferrari, L. Yuan, X. Silver, R. Torres, and M. K. Raizada ACE2 gene transfer attenuates hypertension-linked pathophysiological changes in the SHR Physiol Genomics, January 12, 2007; 27(1): 12 - 19. [Abstract] [Full Text] [PDF]
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 J. R. Ingelfinger ACE2: A New Target for Prevention of Diabetic Nephropathy? J. Am. Soc. Nephrol., November 1, 2006; 17(11): 2957 - 2959. [Full Text] [PDF]
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S. Giunti, D. Barit, and M. E. Cooper Mechanisms of Diabetic Nephropathy: Role of Hypertension Hypertension, October 1, 2006; 48(4): 519 - 526. [Full Text] [PDF]
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 M. J Huentelman, J. L Grobe, J. Vazquez, J. M Stewart, A. P Mecca, M. J Katovich, C. M Ferrario, and M. K Raizada Protection from angiotensin II-induced cardiac hypertrophy and fibrosis by systemic lentiviral delivery of ACE2 in rats Exp Physiol, September 1, 2005; 90(5): 783 - 790. [Abstract] [Full Text] [PDF]
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